Cited by An update on the role of ferroptosis in ischemic stroke: from molecular pathways to Neuroprotection

The mechanism of ferroptosis and its related diseases DOI

Shijian Feng, Dan Tang, Yichang Wang

et al.

Molecular Biomedicine, Journal Year: 2023, Volume and Issue: 4(1)

Published: Oct. 16, 2023

Abstract Ferroptosis, a regulated form of cellular death characterized by the iron-mediated accumulation lipid peroxides, provides novel avenue for delving into intersection metabolism, oxidative stress, and disease pathology. We have witnessed mounting fascination with ferroptosis, attributed to its pivotal roles across diverse physiological pathological conditions including developmental processes, metabolic dynamics, oncogenic pathways, neurodegenerative cascades, traumatic tissue injuries. By unraveling intricate underpinnings molecular machinery, contributors, signaling conduits, regulatory networks governing researchers aim bridge gap between intricacies this unique mode multifaceted implications health disease. In light rapidly advancing landscape ferroptosis research, we present comprehensive review aiming at extensive in origins progress human diseases. This concludes careful analysis potential treatment approaches carefully designed either inhibit or promote ferroptosis. Additionally, succinctly summarized therapeutic targets compounds that hold promise targeting within various facet underscores burgeoning possibilities manipulating as strategy. summary, enriched insights both investigators practitioners, while fostering an elevated comprehension latent translational utilities. revealing basic processes investigating possibilities, crucial resource scientists medical aiding deep understanding effects situations.

Language: Английский

Citations

The Interplay between Ferroptosis and Neuroinflammation in Central Neurological Disorders DOI

Yejia Xu,

Bowen Jia,

Jing Li

et al.

Antioxidants, Journal Year: 2024, Volume and Issue: 13(4), P. 395 - 395

Published: March 26, 2024

Central neurological disorders are significant contributors to morbidity, mortality, and long-term disability globally in modern society. These encompass neurodegenerative diseases, ischemic brain traumatic injury, epilepsy, depression, more. The involved pathogenesis is notably intricate diverse. Ferroptosis neuroinflammation play pivotal roles elucidating the causes of cognitive impairment stemming from these diseases. Given concurrent occurrence ferroptosis due metabolic shifts such as iron ROS, well their critical central nervous disorders, investigation into co-regulatory mechanism has emerged a prominent area research. This paper delves mechanisms along with interrelationship. It specifically emphasizes core molecules within shared pathways governing neuroinflammation, including SIRT1, Nrf2, NF-κB, Cox-2, iNOS/NO·, how different immune cells structures contribute dysfunction through mechanisms. Researchers’ findings suggest that mutually promote each other may represent key factors progression disorders. A deeper comprehension common pathway between cellular holds promise for improving symptoms prognosis related

Language: Английский

Citations

Edaravone dextranol alleviates ferroptosis, Cuproptosis, and blood-brain barrier damage after acute cerebral infarction DOI

Guishan Jin, Wenfeng Han, Tingting Duan

et al.

Metabolic Brain Disease, Journal Year: 2025, Volume and Issue: 40(3)

Published: March 3, 2025

Language: Английский

Citations

Progress of Ferroptosis in Ischemic Stroke and Therapeutic Targets DOI

Xinjuan Tian, Xiang Li, Mengtian Pan

et al.

Cellular and Molecular Neurobiology, Journal Year: 2024, Volume and Issue: 44(1)

Published: Feb. 23, 2024

Ferroptosis is an iron-dependent form of programmed cell death (PCD) and ischemic stroke (IS) has been confirmed to be closely related ferroptosis. The mechanisms ferroptosis were summarized into three interrelated aspects: iron metabolism, lipid peroxide as well glutathione amino acid metabolism. What's more, the causal relationship between IS elucidated by several processes. disruption blood-brain barrier, release excitatory acids, inflammatory response after all lead disorder metabolism antioxidant system. Based on these statements, we reviewed reported effects compounds drugs treating modulating key molecules in Through detailed analysis roles molecules, have also more clearly demonstrated essential effect occurrence so provide new targets ideas for therapeutic IS.

Language: Английский

Citations

Ferroptosis: a potential therapeutic target for stroke DOI

Chengli Liu, Guijun Wang, Wenrui Han

et al.

Neural Regeneration Research, Journal Year: 2023, Volume and Issue: 19(5), P. 988 - 997

Published: Sept. 22, 2023

Ferroptosis is a form of regulated cell death characterized by massive iron accumulation and iron-dependent lipid peroxidation, differing from apoptosis, necroptosis, autophagy in several aspects. regarded as critical mechanism series pathophysiological reactions after stroke because overload caused hemoglobin degradation metabolism imbalance. In this review, we discuss ferroptosis-related metabolisms, important molecules directly or indirectly targeting transcriptional regulation ferroptosis, revealing the role ferroptosis progression stroke. We present updated progress intervention therapeutic strategies for vivo vitro summarize effects inhibitors on Our review facilitates further understanding pathogenesis stroke, proposes new targets treatment suggests that more efforts should be made to investigate

Language: Английский

Citations

DL-3-n-Butylphthalide Ameliorates Post-stroke Emotional Disorders by Suppressing Neuroinflammation and PANoptosis DOI

Yanhui Cui,

Zhaolan Hu,

Laifa Wang

et al.

Neurochemical Research, Journal Year: 2024, Volume and Issue: 49(8), P. 2215 - 2227

Published: June 4, 2024

Language: Английский

Citations

Ferrostatin‑1 alleviates liver injury via decreasing ferroptosis following ricin toxin poisoning in rat DOI

Ruijiao Lin,

Zijie Jia,

Hongbing Chen

et al.

Toxicology, Journal Year: 2024, Volume and Issue: 503, P. 153767 - 153767

Published: March 1, 2024

Ricin is a highly toxic plant toxin that can cause multi-organ failure, especially liver dysfunction, and potential bioterrorism agent. Despite the serious public health challenge posed by ricin, effective therapeutic for ricin-induced poisoning currently unavailable. Therefore, it important to explore mechanism of ricin develop appropriate treatment protocols accordingly. Previous studies have shown lipid peroxidation iron accumulation are associated with poisoning. Ferroptosis an iron-dependent form cell death caused excessive peroxide. The role ferroptosis in unclear require further study. We investigated effect on injury elucidated mechanism. results showed occurred ricin-intoxicated rats, Ferrostatin‑1 could ameliorate hepatic thus injury. induced decreasing reduced glutathione protein level peroxidase 4 Solute Carrier Family 7 Member 11, increasing iron, malondialdehyde reactive oxygen species, mitochondrial damage, whereas pretreatment increased decreased malondialdehyde, ameliorated thereby alleviated These suggested exacerbated after inhibition may be novel strategy

Language: Английский

Citations

Neuroprotective effects of ethanol extraction from Rubia yunnanensis Diels on chronic cerebral hypoperfusion: modulation of the System Xc-/GSH/GPX4 axis to alleviate oxidative stress and ferroptosis DOI

Jianghao Cheng,

Xiao-Xia Ma,

Jie Tao

et al.

Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 16

Published: Feb. 25, 2025

Vascular dementia (VD) is a neurodegenerative disease caused by chronic cerebral hypoperfusion (CCH), which considerably impact patients' quality of life. Ethanol extraction from Rubia yunnanensis (RY-A) has gained attention for its potential neuroprotective effects, but effects and mechanisms action on CCH are unknown. After 30 days RY-A gavage treatment in rat model, were evaluated using the Morris water maze test, blood flow measurements, HE staining brain. These findings, combined with serum medicinal chemistry, RNA-seq, metabolomics analyses, revealed active compounds rats. The results further validated assay kits Western blot techniques. significantly attenuated neurological damage improved cognitive function Ultra-high-performance liquid chromatography high-resolution mass spectrometry identified 511 blood-entry RY-A. RNA-seq metabolomic analysis showed that might help to normalize changes gene metabolite expression CCH. induced increasing production key proteins involved ferroptosis inhibition, such as SLC7A11, SLC3A2, GSS, GPX4, while antioxidant enzyme activities alleviating oxidative stress. inhibited stress activating System Xc-/GSH/GPX4 pathway balancing iron metabolism, thereby attenuating CCH-induced deficits.

Language: Английский

Citations

Population Pharmacokinetics of Butylphthalide Injection in Elderly Chinese Patients With Ischemic Stroke DOI

Shu‐Xian Lyu,

Xueyan Cui,

Shixian Chen

et al.

Clinical Pharmacology in Drug Development, Journal Year: 2025, Volume and Issue: unknown

Published: March 28, 2025

Abstract Butylphthalide is widely used to treat acute ischemic stroke in China, and the main adverse effect increase transaminase levels. We aimed establish a population pharmacokinetic model of butylphthalide elderly patients with identified covariates influencing pharmacokinetics. collected blood samples via opportunistic sampling. chose base model, compared 1‐, 2‐, 3‐compartment models, basic patient information, laboratory test results, concomitant drugs, comorbidities as examine our study. Our study included 50 (n = 106 samples), 2‐compartment first‐order elimination matched experimental data well. Body weight comorbid diabetes significantly affect clearance butylphthalide. On basis final PPK Monte Carlo method was compare effects different body weights state on steady‐state area under concentration–time curve at 0‐24 hours. The results revealed that hours lower than without diabetes, both values decreased gain. findings provide information for personalized treatment plans (aged 65 years or older) receiving injection.

Language: Английский

Citations

Dl-3-n-Butylphthalide Promotes Neurogenesis in Ischemic Stroke Mice Through Wnt/β-Catenin Signaling Activation and Neurotrophic Factor Production DOI

Lan Zhang, Cong Zhang, Rong Chen

et al.

Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown

Published: April 2, 2025

Synchronized neurogenesis and angiogenesis after stroke have been well documented, inducing neurovascular remodeling may provide a promising strategy to promote tissue repair functional recovery. Dl-3-n-Butylphthalide (NBP) was reported exert potent angiogenic activity in rodent models of stroke. However, little is currently known regarding the effects mechanisms NBP on ischemic This study aimed determine whether how promotes cerebral injury. Adult C57BL/6 mice, subjected distal middle artery occlusion (dMCAO), were treated with NBP. The efficacy assessed using neurologic deficits infarct volume. Immunofluorescent staining applied evaluate neurogenesis. regulation Wnt/β-catenin signaling pathway expression neurotrophic factors detected by western blotting qRT-PCR. Administration reduced volume ameliorated neurological promoted proliferation NSCs SVZ, migration neuroblasts along corpus callosum, differentiation toward neurons peri-infarct zone, resulting restored neural function. Moreover, we revealed that NBP-induced associated activation pathway, which reversed DKK1. In addition, increased production VEGF BDNF. Our data unveiled potentials recovery stroke, depending factor production. Thus, be candidate for delayed treatment

Language: Английский

Citations